Supplementary Files Identification and Validation of Hypoxia-Derived Gene
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The RNA Response to DNA Damage
ÔØ ÅÒÙ×Ö ÔØ The RNA response to DNA damage Luciana E. Giono, Nicol´as Nieto Moreno, Adri´an E. Cambindo Botto, Gwendal Dujardin, Manuel J. Mu˜noz, Alberto R. Kornblihtt PII: S0022-2836(16)00177-7 DOI: doi: 10.1016/j.jmb.2016.03.004 Reference: YJMBI 65022 To appear in: Journal of Molecular Biology Received date: 10 December 2015 Revised date: 1 March 2016 Accepted date: 7 March 2016 Please cite this article as: Giono, L.E., Moreno, N.N., Botto, A.E.C., Dujardin, G., Mu˜noz, M.J. & Kornblihtt, A.R., The RNA response to DNA damage, Journal of Molec- ular Biology (2016), doi: 10.1016/j.jmb.2016.03.004 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ACCEPTED MANUSCRIPT The RNA response to DNA damage Luciana E. Giono1, Nicolás Nieto Moreno1, Adrián E. Cambindo Botto1, Gwendal Dujardin1,2, Manuel J. Muñoz1, and Alberto R. Kornblihtt1* 1Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-UBA-CONICET) and Departamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Pabellón 2, C1428EHA Buenos Aires, Argentina 2Centre for GenomicACCEPTED Regulation. Dr. -
VAMP3 and VAMP8 Regulate the Development and Functionality of 5 Parasitophorous Vacuoles Housing Leishmania Amazonensis
bioRxiv preprint doi: https://doi.org/10.1101/2020.07.09.195032; this version posted July 9, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 2 3 4 VAMP3 and VAMP8 regulate the development and functionality of 5 parasitophorous vacuoles housing Leishmania amazonensis 6 7 8 Olivier Séguin1, Linh Thuy Mai1, Sidney W. Whiteheart2, Simona Stäger1, Albert Descoteaux1* 9 10 11 12 1Institut national de la recherche scientifique, Centre Armand-Frappier Santé Biotechnologie, 13 Laval, Québec, Canada 14 15 2Department of Molecular and Cellular Biochemistry, University of Kentucky College of 16 Medicine, Lexington, Kentucky, United States of America 17 18 19 *Corresponding author: 20 E-mail: [email protected] 21 22 23 24 Short title: SNAREs and Leishmania-harboring communal parasitophorous vacuoles 25 bioRxiv preprint doi: https://doi.org/10.1101/2020.07.09.195032; this version posted July 9, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 26 ABSTRACT 27 28 To colonize mammalian phagocytic cells, the parasite Leishmania remodels phagosomes into 29 parasitophorous vacuoles that can be either tight-fitting individual or communal. The molecular 30 and cellular bases underlying the biogenesis and functionality of these two types of vacuoles are 31 poorly understood. -
Gene Symbol Gene Description ACVR1B Activin a Receptor, Type IB
Table S1. Kinase clones included in human kinase cDNA library for yeast two-hybrid screening Gene Symbol Gene Description ACVR1B activin A receptor, type IB ADCK2 aarF domain containing kinase 2 ADCK4 aarF domain containing kinase 4 AGK multiple substrate lipid kinase;MULK AK1 adenylate kinase 1 AK3 adenylate kinase 3 like 1 AK3L1 adenylate kinase 3 ALDH18A1 aldehyde dehydrogenase 18 family, member A1;ALDH18A1 ALK anaplastic lymphoma kinase (Ki-1) ALPK1 alpha-kinase 1 ALPK2 alpha-kinase 2 AMHR2 anti-Mullerian hormone receptor, type II ARAF v-raf murine sarcoma 3611 viral oncogene homolog 1 ARSG arylsulfatase G;ARSG AURKB aurora kinase B AURKC aurora kinase C BCKDK branched chain alpha-ketoacid dehydrogenase kinase BMPR1A bone morphogenetic protein receptor, type IA BMPR2 bone morphogenetic protein receptor, type II (serine/threonine kinase) BRAF v-raf murine sarcoma viral oncogene homolog B1 BRD3 bromodomain containing 3 BRD4 bromodomain containing 4 BTK Bruton agammaglobulinemia tyrosine kinase BUB1 BUB1 budding uninhibited by benzimidazoles 1 homolog (yeast) BUB1B BUB1 budding uninhibited by benzimidazoles 1 homolog beta (yeast) C9orf98 chromosome 9 open reading frame 98;C9orf98 CABC1 chaperone, ABC1 activity of bc1 complex like (S. pombe) CALM1 calmodulin 1 (phosphorylase kinase, delta) CALM2 calmodulin 2 (phosphorylase kinase, delta) CALM3 calmodulin 3 (phosphorylase kinase, delta) CAMK1 calcium/calmodulin-dependent protein kinase I CAMK2A calcium/calmodulin-dependent protein kinase (CaM kinase) II alpha CAMK2B calcium/calmodulin-dependent -
The Rise and Fall of the Bovine Corpus Luteum
University of Nebraska Medical Center DigitalCommons@UNMC Theses & Dissertations Graduate Studies Spring 5-6-2017 The Rise and Fall of the Bovine Corpus Luteum Heather Talbott University of Nebraska Medical Center Follow this and additional works at: https://digitalcommons.unmc.edu/etd Part of the Biochemistry Commons, Molecular Biology Commons, and the Obstetrics and Gynecology Commons Recommended Citation Talbott, Heather, "The Rise and Fall of the Bovine Corpus Luteum" (2017). Theses & Dissertations. 207. https://digitalcommons.unmc.edu/etd/207 This Dissertation is brought to you for free and open access by the Graduate Studies at DigitalCommons@UNMC. It has been accepted for inclusion in Theses & Dissertations by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. THE RISE AND FALL OF THE BOVINE CORPUS LUTEUM by Heather Talbott A DISSERTATION Presented to the Faculty of the University of Nebraska Graduate College in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Biochemistry and Molecular Biology Graduate Program Under the Supervision of Professor John S. Davis University of Nebraska Medical Center Omaha, Nebraska May, 2017 Supervisory Committee: Carol A. Casey, Ph.D. Andrea S. Cupp, Ph.D. Parmender P. Mehta, Ph.D. Justin L. Mott, Ph.D. i ACKNOWLEDGEMENTS This dissertation was supported by the Agriculture and Food Research Initiative from the USDA National Institute of Food and Agriculture (NIFA) Pre-doctoral award; University of Nebraska Medical Center Graduate Student Assistantship; University of Nebraska Medical Center Exceptional Incoming Graduate Student Award; the VA Nebraska-Western Iowa Health Care System Department of Veterans Affairs; and The Olson Center for Women’s Health, Department of Obstetrics and Gynecology, Nebraska Medical Center. -
Genetic and Epigenetic Determinants of Thrombin Generation Potential : an Epidemiological Approach Maria-Ares Rocanin-Arjo
Genetic and Epigenetic Determinants of Thrombin Generation Potential : an epidemiological approach Maria-Ares Rocanin-Arjo To cite this version: Maria-Ares Rocanin-Arjo. Genetic and Epigenetic Determinants of Thrombin Generation Potential : an epidemiological approach. Génétique humaine. Université Paris Sud - Paris XI, 2014. Français. NNT : 2014PA11T067. tel-01231859 HAL Id: tel-01231859 https://tel.archives-ouvertes.fr/tel-01231859 Submitted on 21 Nov 2015 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. UNIVERSITÉ PARIS-SUD ÉCOLE DOCTORALE 420 : SANTÉ PUBLIQUE PARIS SUD 11, PARIS DESCARTES Laboratoire : Equip 1 de Unité INSERM UMR_S1166 Genomics & Pathophysiology of Cardiovascular Diseases THÈSE DE DOCTORAT SANTÉ PUBLIQUE - GÉNÉTIQUE STATISTIQUE par Ares ROCAÑIN ARJO Genetic and Epigenetic Determinants of Thrombin Generation Potential: an epidemiological approach. Date de soutenance : 20/11/2014 Composition du jury : Directeur de thèse : David Alexandre TREGOUET DR, INSERM U1166, Université Paris 6, Jussieu Rapporteurs : Guy MEYER PU_PH, Service de pneumologie. Hôpital européen Georges Pompidou Richard REDON DR, Institut thorax, UMR 1087 / CNRS UMR 6291 , Université de Nantes Examinateurs : Laurent ABEL DR, INSERM U980, Institut Imagine Marie Aline CHARLES DR, INSERM U1018, CESP Al meu pare (to my father /à mon père) Your genetics load the gun. -
Stimulating the Expression of Sphingosine Kinase 1 (Sphk1) Is Bene Cial to Reduce Acrylamide-Induced Nerve Cell Damage
Stimulating the Expression of Sphingosine Kinase 1 (SphK1) is Benecial to Reduce Acrylamide-Induced Nerve Cell Damage Yong-Hui Wu ( [email protected] ) Harbin Medical University https://orcid.org/0000-0002-4838-2947 Sheng-Yuan Wang Harbin Medical University Xiao-Li Wang Harbin Medical University Rui Xin Harbin Medical University Ye Xin Harbin Medical University Rui Wang Harbin Medical University Kun Ma Harbin Medical University Cui-Ping Yu Harbin Medical University Dan Zhang Harbin Medical University Xiao-Rong Zhou Harbin Medical University Wei-Wei Ma Harbin Medical University Chao Wang Harbin Medical University Research Keywords: Acrylamide, SphKl, Neurotoxicity, Apoptosis, MAPK pathway Posted Date: September 28th, 2020 DOI: https://doi.org/10.21203/rs.3.rs-80914/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Stimulating the expression of sphingosine kinase 1 (SphK1) is beneficial to reduce acrylamide-induced nerve cell damage Sheng-Yuan Wang1, Xiao-Li Wang1, Rui Xin1, Ye Xin1, Rui Wang1, Kun Ma2, Cui-Ping Yu1, Dan Zhang1, Xiao-Rong Zhou1, Wei-Wei Ma3, Chao Wang4, Yong-Hui Wu1* 1 Department of Occupational Health, Public Health College, Harbin Medical University, Harbin, P. R. 2 Department of Hygienic Toxicology, Public Health College, Harbin Medical University, Harbin, P. R. 3 Harbin Railway Center for Disease Control and Prevention, Harbin, P. R. 4 Health Commission of Heilongjiang Province. * Address correspondence to this author at: The Department of Occupational Health, Public Health College, Harbin Medical University, 157 Baojian Road, Nan gang District, Harbin, People’s Republic of China 150086. Phone: +86-451-8750-2827, Fax: +86-451-8750-2827, E-mail: [email protected]. -
Dual Proteome-Scale Networks Reveal Cell-Specific Remodeling of the Human Interactome
bioRxiv preprint doi: https://doi.org/10.1101/2020.01.19.905109; this version posted January 19, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Dual Proteome-scale Networks Reveal Cell-specific Remodeling of the Human Interactome Edward L. Huttlin1*, Raphael J. Bruckner1,3, Jose Navarrete-Perea1, Joe R. Cannon1,4, Kurt Baltier1,5, Fana Gebreab1, Melanie P. Gygi1, Alexandra Thornock1, Gabriela Zarraga1,6, Stanley Tam1,7, John Szpyt1, Alexandra Panov1, Hannah Parzen1,8, Sipei Fu1, Arvene Golbazi1, Eila Maenpaa1, Keegan Stricker1, Sanjukta Guha Thakurta1, Ramin Rad1, Joshua Pan2, David P. Nusinow1, Joao A. Paulo1, Devin K. Schweppe1, Laura Pontano Vaites1, J. Wade Harper1*, Steven P. Gygi1*# 1Department of Cell Biology, Harvard Medical School, Boston, MA, 02115, USA. 2Broad Institute, Cambridge, MA, 02142, USA. 3Present address: ICCB-Longwood Screening Facility, Harvard Medical School, Boston, MA, 02115, USA. 4Present address: Merck, West Point, PA, 19486, USA. 5Present address: IQ Proteomics, Cambridge, MA, 02139, USA. 6Present address: Vor Biopharma, Cambridge, MA, 02142, USA. 7Present address: Rubius Therapeutics, Cambridge, MA, 02139, USA. 8Present address: RPS North America, South Kingstown, RI, 02879, USA. *Correspondence: [email protected] (E.L.H.), [email protected] (J.W.H.), [email protected] (S.P.G.) #Lead Contact: [email protected] bioRxiv preprint doi: https://doi.org/10.1101/2020.01.19.905109; this version posted January 19, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Protein Identities in Evs Isolated from U87-MG GBM Cells As Determined by NG LC-MS/MS
Protein identities in EVs isolated from U87-MG GBM cells as determined by NG LC-MS/MS. No. Accession Description Σ Coverage Σ# Proteins Σ# Unique Peptides Σ# Peptides Σ# PSMs # AAs MW [kDa] calc. pI 1 A8MS94 Putative golgin subfamily A member 2-like protein 5 OS=Homo sapiens PE=5 SV=2 - [GG2L5_HUMAN] 100 1 1 7 88 110 12,03704523 5,681152344 2 P60660 Myosin light polypeptide 6 OS=Homo sapiens GN=MYL6 PE=1 SV=2 - [MYL6_HUMAN] 100 3 5 17 173 151 16,91913397 4,652832031 3 Q6ZYL4 General transcription factor IIH subunit 5 OS=Homo sapiens GN=GTF2H5 PE=1 SV=1 - [TF2H5_HUMAN] 98,59 1 1 4 13 71 8,048185945 4,652832031 4 P60709 Actin, cytoplasmic 1 OS=Homo sapiens GN=ACTB PE=1 SV=1 - [ACTB_HUMAN] 97,6 5 5 35 917 375 41,70973209 5,478027344 5 P13489 Ribonuclease inhibitor OS=Homo sapiens GN=RNH1 PE=1 SV=2 - [RINI_HUMAN] 96,75 1 12 37 173 461 49,94108966 4,817871094 6 P09382 Galectin-1 OS=Homo sapiens GN=LGALS1 PE=1 SV=2 - [LEG1_HUMAN] 96,3 1 7 14 283 135 14,70620005 5,503417969 7 P60174 Triosephosphate isomerase OS=Homo sapiens GN=TPI1 PE=1 SV=3 - [TPIS_HUMAN] 95,1 3 16 25 375 286 30,77169764 5,922363281 8 P04406 Glyceraldehyde-3-phosphate dehydrogenase OS=Homo sapiens GN=GAPDH PE=1 SV=3 - [G3P_HUMAN] 94,63 2 13 31 509 335 36,03039959 8,455566406 9 Q15185 Prostaglandin E synthase 3 OS=Homo sapiens GN=PTGES3 PE=1 SV=1 - [TEBP_HUMAN] 93,13 1 5 12 74 160 18,68541938 4,538574219 10 P09417 Dihydropteridine reductase OS=Homo sapiens GN=QDPR PE=1 SV=2 - [DHPR_HUMAN] 93,03 1 1 17 69 244 25,77302971 7,371582031 11 P01911 HLA class II histocompatibility antigen, -
Supplementary Table 4
Li et al. mir-30d in human cancer Table S4. The probe list down-regulated in MDA-MB-231 cells by mir-30d mimic transfection Gene Probe Gene symbol Description Row set 27758 8119801 ABCC10 ATP-binding cassette, sub-family C (CFTR/MRP), member 10 15497 8101675 ABCG2 ATP-binding cassette, sub-family G (WHITE), member 2 18536 8158725 ABL1 c-abl oncogene 1, receptor tyrosine kinase 21232 8058591 ACADL acyl-Coenzyme A dehydrogenase, long chain 12466 7936028 ACTR1A ARP1 actin-related protein 1 homolog A, centractin alpha (yeast) 18102 8056005 ACVR1 activin A receptor, type I 20790 8115490 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 15688 7979904 ADAM21 ADAM metallopeptidase domain 21 14937 8054254 AFF3 AF4/FMR2 family, member 3 23560 8121277 AIM1 absent in melanoma 1 20209 7921434 AIM2 absent in melanoma 2 19272 8136336 AKR1B10 aldo-keto reductase family 1, member B10 (aldose reductase) 18013 7954777 ALG10 asparagine-linked glycosylation 10, alpha-1,2-glucosyltransferase homolog (S. pombe) 30049 7954789 ALG10B asparagine-linked glycosylation 10, alpha-1,2-glucosyltransferase homolog B (yeast) 28807 7962579 AMIGO2 adhesion molecule with Ig-like domain 2 5576 8112596 ANKRA2 ankyrin repeat, family A (RFXANK-like), 2 23414 7922121 ANKRD36BL1 ankyrin repeat domain 36B-like 1 (pseudogene) 29782 8098246 ANXA10 annexin A10 22609 8030470 AP2A1 adaptor-related protein complex 2, alpha 1 subunit 14426 8107421 AP3S1 adaptor-related protein complex 3, sigma 1 subunit 12042 8099760 ARAP2 ArfGAP with RhoGAP domain, ankyrin repeat and PH domain 2 30227 8059854 ARL4C ADP-ribosylation factor-like 4C 32785 8143766 ARP11 actin-related Arp11 6497 8052125 ASB3 ankyrin repeat and SOCS box-containing 3 24269 8128592 ATG5 ATG5 autophagy related 5 homolog (S. -
Cellular and Molecular Signatures in the Disease Tissue of Early
Cellular and Molecular Signatures in the Disease Tissue of Early Rheumatoid Arthritis Stratify Clinical Response to csDMARD-Therapy and Predict Radiographic Progression Frances Humby1,* Myles Lewis1,* Nandhini Ramamoorthi2, Jason Hackney3, Michael Barnes1, Michele Bombardieri1, Francesca Setiadi2, Stephen Kelly1, Fabiola Bene1, Maria di Cicco1, Sudeh Riahi1, Vidalba Rocher-Ros1, Nora Ng1, Ilias Lazorou1, Rebecca E. Hands1, Desiree van der Heijde4, Robert Landewé5, Annette van der Helm-van Mil4, Alberto Cauli6, Iain B. McInnes7, Christopher D. Buckley8, Ernest Choy9, Peter Taylor10, Michael J. Townsend2 & Costantino Pitzalis1 1Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Departments of 2Biomarker Discovery OMNI, 3Bioinformatics and Computational Biology, Genentech Research and Early Development, South San Francisco, California 94080 USA 4Department of Rheumatology, Leiden University Medical Center, The Netherlands 5Department of Clinical Immunology & Rheumatology, Amsterdam Rheumatology & Immunology Center, Amsterdam, The Netherlands 6Rheumatology Unit, Department of Medical Sciences, Policlinico of the University of Cagliari, Cagliari, Italy 7Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK 8Rheumatology Research Group, Institute of Inflammation and Ageing (IIA), University of Birmingham, Birmingham B15 2WB, UK 9Institute of -
Lipid Metabolic Reprogramming: Role in Melanoma Progression and Therapeutic Perspectives
cancers Review Lipid metabolic Reprogramming: Role in Melanoma Progression and Therapeutic Perspectives 1, 1, 1 2 1 Laurence Pellerin y, Lorry Carrié y , Carine Dufau , Laurence Nieto , Bruno Ségui , 1,3 1, , 1, , Thierry Levade , Joëlle Riond * z and Nathalie Andrieu-Abadie * z 1 Centre de Recherches en Cancérologie de Toulouse, Equipe Labellisée Fondation ARC, Université Fédérale de Toulouse Midi-Pyrénées, Université Toulouse III Paul-Sabatier, Inserm 1037, 2 avenue Hubert Curien, tgrCS 53717, 31037 Toulouse CEDEX 1, France; [email protected] (L.P.); [email protected] (L.C.); [email protected] (C.D.); [email protected] (B.S.); [email protected] (T.L.) 2 Institut de Pharmacologie et de Biologie Structurale, CNRS, Université Toulouse III Paul-Sabatier, UMR 5089, 205 Route de Narbonne, 31400 Toulouse, France; [email protected] 3 Laboratoire de Biochimie Métabolique, CHU Toulouse, 31059 Toulouse, France * Correspondence: [email protected] (J.R.); [email protected] (N.A.-A.); Tel.: +33-582-7416-20 (J.R.) These authors contributed equally to this work. y These authors jointly supervised this work. z Received: 15 September 2020; Accepted: 23 October 2020; Published: 27 October 2020 Simple Summary: Melanoma is a devastating skin cancer characterized by an impressive metabolic plasticity. Melanoma cells are able to adapt to the tumor microenvironment by using a variety of fuels that contribute to tumor growth and progression. In this review, the authors summarize the contribution of the lipid metabolic network in melanoma plasticity and aggressiveness, with a particular attention to specific lipid classes such as glycerophospholipids, sphingolipids, sterols and eicosanoids.